Obstructive sleep apnea is a common disorder characterized by intermittent collapse of the pharyngeal airway during sleep with important physiologic (systemic and pulmonary hypertension, arrhythmias, probably decreased survival) and neuropsychological (waking hypersomnolence) sequelae. Pharyngeal patency during both wakefulness and sleep is likely a product of both the structural and functional characteristics of the individual upper airway with pharyngeal dilator muscles playing an important role in maintaining airway patency. We have developed a series of hypotheses that are strongly supported by our preliminary data which we believe explain first the known increment in upper airway resistance that occurs during sleep in normal subjects and second the complete upper airway collapse characteristic of sleep apnea. the principle components of these hypotheses are: (A) Sleep has a non-uniform influence of pharyngeal muscle activity with a maintenance of activity in muscles with prominent inspiratory phasic activity (controlled by central respiratory neurons: example - genioglossus) and a marked decrement in the activity of tonic postural muscles (little influence from central respiratory neurons: example - tensor palatini). (B) The activity of these pharyngeal dilator muscles is controlled by both chemical (PCO2, PO2) and neural reflex (negative pressure, airway collapse) mechanisms. Loss of neural reflex mechanisms occurs during NREM sleep while chemical mechanisms are reasonably maintained. (C) Loss of activity in the tonic postural muscles of the palate is the principle cause of increasing airflow resistance during sleep in normals. (D) Apnea patients, as described by others, have an anatomically small airway. However, during wakefulness they maintain patency by increased pharyngeal dilator muscle activity (neuromuscular compensation). (E) During sleep, neuromuscular compensatory mechanisms (neural reflexes) are lost in apnea patients leading to a fall in muscle activity and airway collapse. We have, in our laboratory, developed the techniques and methodology needed to first quantify the electrical activity of the various pharyngeal dilator muscles during both wakefulness and sleep and second the ability to compare this muscle activity between individuals. this should allow us to test all the hypotheses described above. At this time our understanding of normal pharyngeal muscle function both awake and asleep is in its infancy and it is only by understanding the normal physiology of these muscles that the pathology in sleep apnea can be appreciated. We, therefore, propose to carefully study the normal respiratory role of the pharyngeal muscles during wakefulness and sleep with a particular focus on the palate. Subsequent studies will be aimed at sleep apnea patients to determine how and why their pharyngeal airway performs differently from the normal individual.